domingo, dezembro 30, 2012

Higgs boson theorist says he agrees with those who find Dawkins' approach to dealing with believers 'embarrassing'

Alok Jha, science correspondent

The Guardian, Wednesday 26 December 2012 18.58 GMT

As public disagreements go, few can have boasted such heavy-hitting antagonists.

On one side is Richard Dawkins, the celebrated biologist who has made a second career demonstrating his epic disdain for religion. On the other is the theoretical physicist Peter Higgs, who this year became a shoo-in for a future Nobel prize after scientists at Cern in Geneva showed that his theory about how fundamental particles get their mass was correct.

Their argument is over nothing less than the coexistence of religion and science.

Higgs has chosen to cap his remarkable 2012 with another bang by criticising the "fundamentalist" approach taken by Dawkins in dealing with religious believers.

"What Dawkins does too often is to concentrate his attack on fundamentalists. But there are many believers who are just not fundamentalists," Higgs said in an interview with the Spanish newspaper El Mundo. "Fundamentalism is another problem. I mean, Dawkins in a way is almost a fundamentalist himself, of another kind."

He agreed with some of Dawkins' thoughts on the unfortunate consequences that have resulted from religious belief, but he was unhappy with the evolutionary biologist's approach to dealing with believers and said he agreed with those who found Dawkins' approach "embarrassing".

Dawkins, author of the best-selling book The God Delusion, has been accused many times in the past of adopting fundamentalist positions.. In a 2007 post on his website titled "How dare you call me a fundamentalist", Dawkins wrote: "No, please, do not mistake passion, which can change its mind, for fundamentalism, which never will. Passion for passion, an evangelical Christian and I may be evenly matched. But we are not equally fundamentalist. The true scientist, however passionately he may 'believe', in evolution for example, knows exactly what would change his mind: evidence! The fundamentalist knows that nothing will."

The criticisms have not led the biologist to soften his stance on religion. In a recent interview with al-Jazeera, he implied that being raised a Catholic was worse for a child than physical abuse by a priest. Responding to a direct question from the interviewer Mehdi Hassan, Dawkins related the story of a woman in America who had written to him about abuse she suffered as a child at the hands of a priest, and the mental anguish of being told that one of her friends, a Protestant girl, would burn in hell.

"She told me that, of those two abuses, she got over the physical abuse, it was yucky but she got over it. But the mental abuse of being told about hell, she took years to get over," said Dawkins. "Telling children such that they really, really believe that people who sin are going to go to hell and roast forever, that your skin grows again when it peels off, it seems to me intuitively entirely reasonable that that is a worse form of child abuse, that will give more nightmares because they really believe it."

Dawkins did not respond to a request to comment directly on Higgs's "fundamentalist" charge.

In the El Mundo interview, Higgs argued that although he was not a believer, he thought science and religion were not incompatible. "The growth of our understanding of the world through science weakens some of the motivation which makes people believers. But that's not the same thing as saying they're incompatible. It's just that I think some of the traditional reasons for belief, going back thousands of years, are rather undermined.

"But that doesn't end the whole thing. Anybody who is a convinced but not a dogmatic believer can continue to hold his belief. It means I think you have to be rather more careful about the whole debate between science and religion than some people have been in the past."

He said a lot of scientists in his field were religious believers. "I don't happen to be one myself, but maybe that's just more a matter of my family background than that there's any fundamental difficulty about reconciling the two."

sexta-feira, dezembro 28, 2012

Phil. Trans. R. Soc. Lond. B

14 August 1952 vol. 237 no. 641 37-72

The Chemical Basis of Morphogenesis

A. M. Turing

Abstract

It is suggested that a system of chemical substances, called morphogens, reacting together and diffusing through a tissue, is adequate to account for the main phenomena of morphogenesis. Such a system, although it may originally be quite homogeneous, may later develop a pattern or structure due to an instability of the homogeneous equilibrium, which is triggered off by random disturbances. Such reaction-diffusion systems are considered in some detail in the case of an isolated ring of cells, a mathematically convenient, though biologically unusual system. The investigation is chiefly concerned with the onset of instability. It is found that there are six essentially different forms which this may take. In the most interesting form stationary waves appear on the ring. It is suggested that this might account, for instance, for the tentacle patterns on Hydra and for whorled leaves. A system of reactions and diffusion on a sphere is also considered. Such a system appears to account for gastrulation. Another reaction system in two dimensions gives rise to patterns reminiscent of dappling. It is also suggested that stationary waves in two dimensions could account for the phenomena of phyllotaxis. The purpose of this paper is to discuss a possible mechanism by which the genes of a zygote may determine the anatomical structure of the resulting organism. The theory does not make any new hypotheses; it merely suggests that certain well-known physical laws are sufficient to account for many of the facts. The full understanding of the paper requires a good knowledge of mathematics, some biology, and some elementary chemistry. Since readers cannot be expected to be experts in all of these subjects, a number of elementary facts are explained, which can be found in text-books, but whose omission would make the paper difficult reading.

Sixty years ago, noted mathematician Alan Turing described how two interacting chemicals diffusing through space could form interacting wave patterns. Recently, experiments have suggested that Turing's mechanisms play a role in the growth of feathers, hair follicles, the branching pattern of lungs, and even the left-right asymmetry that puts the heart on the left side of the chest. In this issue of Science, a team of biologists offer fresh evidence that this theory guides how some parts of the body develop, as Turing's model also appears to describe the pattern that leads to digit formation in the developing mouse paw.

The formation of repetitive structures (such as stripes) in nature is often consistent with a reaction-diffusion mechanism, or Turing model, of self-organizing systems. We used mouse genetics to analyze how digit patterning (an iterative digit/nondigit pattern) is generated. We showed that the progressive reduction in Hoxa13 and Hoxd11-Hoxd13 genes (hereafter referred to as distal Hox genes) from the Gli3-null background results in progressively more severe polydactyly, displaying thinner and densely packed digits. Combined with computer modeling, our results argue for a Turing-type mechanism underlying digit patterning, in which the dose of distal Hox genes modulates the digit period or wavelength. The phenotypic similarity with fish-fin endoskeleton patterns suggests that the pentadactyl state has been achieved through modification of an ancestral Turing-type mechanism.

The fine-tuning of the universe for intelligent life has received a great deal of attention in recent years, both in the philosophical and scientific literature. The claim is that in the space of possible physical laws, parameters and initial conditions, the set that permits the evolution of intelligent life is very small. I present here a review of the scientific literature, outlining cases of fine-tuning in the classic works of Carter, Carr and Rees, and Barrow and Tipler, as well as more recent work. To sharpen the discussion, the role of the antagonist will be played by Victor Stenger's recent book The Fallacy of Fine-Tuning: Why the Universe is Not Designed for Us. Stenger claims that all known fine-tuning cases can be explained without the need for a multiverse. Many of Stenger's claims will be found to be highly problematic. We will touch on such issues as the logical necessity of the laws of nature; objectivity, invariance and symmetry; theoretical physics and possible universes; entropy in cosmology; cosmic inflation and initial conditions; galaxy formation; the cosmological constant; stars and their formation; the properties of elementary particles and their e fect on chemistry and the macroscopic world; the origin of mass; grand uni fied theories; and the dimensionality of space and time. I also provide an assessment of the multiverse, noting the signi cant challenges that it must face. I do not attempt to defend any conclusion based on the fine-tuning of the universe for intelligent life. This paper can be viewed as a critique of Stenger's book, or read independently.

On the 100th anniversary of Piltdown man, fraud is still a problem in science, writes Seattle Times editorial columnist Bruce Ramsey.

By Bruce Ramsey

Times editorial columnist

Tuesday is the centennial of the grossest fraud of 20th-century science: Piltdown man. It is a case worth remembering.

On Dec. 18, 1912, amateur geologist Charles Dawson presented to the Geological Society of London a partial skull. It was purported to be a human ancestor 500,000 to 1 million years old, an age scientists now assign to Homo erectus. Dawson said he had found the fossils in a gravel pit near Piltdown Common, south of London.

Dawson had no scientific credentials, but his friend Arthur Smith Woodward did. Woodward was the keeper of the geological department at the British Museum. He had been at the dig and had seen the jawbone “fly out” of the ground under the blow of Dawson’s pick.

There was a problem with the jawbone. It was from an orangutan only a few hundred years old. It was fitted with two fossilized chimpanzee teeth, filed down to make them look more like human teeth. The cranium fragments were human, from the Middle Ages. All had been treated with an iron solution and acid to make them look older.

Scientists didn’t have many fossil skulls in 1912, but none of them looked like a human cranium with an ape jaw.

Several scientists, including one from the Smithsonian Institution, argued that the jaw and cranium did not match. It took 40 years for them to be proved right, and even longer for Dawson to be confirmed as the con man responsible.

Science is human. It is subject to error and, what’s more, malice. Unlike some other purported paths to truth, science has a way of detecting errors, but not an automatic way. Someone has to do it.

quarta-feira, dezembro 19, 2012

Fossils, molecules and embryos: new perspectives on the Cambrian explosion.

Valentine JW, Jablonski D, Erwin DH.

Collaborators (1)

Source

Department of Integrative Biology and Museum of Paleontology, University of California, Berkeley, CA 94720, USA. jwv@ucmp1.berkeley.edu

Abstract

The Cambrian explosion is named for the geologically sudden appearance of numerous metazoan body plans (many of living phyla) between about 530 and 520 million years ago, only 1.7% of the duration of the fossil record of animals. Earlier indications of metazoans are found in the Neoproterozic; minute trails suggesting bilaterian activity date from about 600 million years ago. Larger and more elaborate fossil burrows appear near 543 million years ago, the beginning of the Cambrian Period. Evidence of metazoan activity in both trace and body fossils then increased during the 13 million years leading to the explosion. All living phyla may have originated by the end of the explosion. Molecular divergences among lineages leading to phyla record speciation events that have been earlier than the origins of the new body plans, which can arise many tens of millions of years after an initial branching. Various attempts to date those branchings by using molecular clocks have disagreed widely. While the timing of the evolution of the developmental systems of living metazoan body plans is still uncertain, the distribution of Hox and other developmental control genes among metazoans indicates that an extensive patterning system was in place prior to the Cambrian. However, it is likely that much genomic repatterning occurred during the Early Cambrian, involving both key control genes and regulators within their downstream cascades, as novel body plans evolved.

Although it has been notoriously difficult to pin down precisely what it is that makes life so distinctive and remarkable, there is general agreement that its informational aspect is one key property, perhaps the key property. The unique informational narrative of living systems suggests that life may be characterized by context-dependent causal influences, and in particular, that top-down (or downward) causation -- where higher-levels influence and constrain the dynamics of lower-levels in organizational hierarchies -- may be a major contributor to the hierarchal structure of living systems. Here we propose that the origin of life may correspond to a physical transition associated with a shift in causal structure, where information gains direct, and context-dependent causal efficacy over the matter it is instantiated in. Such a transition may be akin to more traditional physical transitions (e.g. thermodynamic phase transitions), with the crucial distinction that determining which phase (non-life or life) a given system is in requires dynamical information and therefore can only be inferred by identifying causal architecture. We discuss some potential novel research directions based on this hypothesis, including potential measures of such a transition that may be amenable to laboratory study, and how the proposed mechanism corresponds to the onset of the unique mode of (algorithmic) information processing characteristic of living systems.

The compositional and evolutionary logic of metabolism

Abstract

Topical Review

Metabolism is built on a foundation of organic chemistry, and employs structures and interactions at many scales. Despite these sources of complexity, metabolism also displays striking and robust regularities in the forms of modularity and hierarchy, which may be described compactly in terms of relatively few principles of composition. These regularities render metabolic architecture comprehensible as a system, and also suggests the order in which layers of that system came into existence. In addition metabolism also serves as a foundational layer in other hierarchies, up to at least the levels of cellular integration including bioenergetics and molecular replication, and trophic ecology. The recapitulation of patterns first seen in metabolism, in these higher levels, motivates us to interpret metabolism as a source of causation or constraint on many forms of organization in the biosphere. Many of the forms of modularity and hierarchy exhibited by metabolism are readily interpreted as stages in the emergence of catalytic control by living systems over organic chemistry, sometimes recapitulating or incorporating geochemical mechanisms.

We identify as modules, either subsets of chemicals and reactions, or subsets of functions, that are re-used in many contexts with a conserved internal structure. At the small molecule substrate level, module boundaries are often associated with the most complex reaction mechanisms, catalyzed by highly conserved enzymes. Cofactors form a biosynthetically and functionally distinctive control layer over the small-molecule substrate. The most complex members among the cofactors are often associated with the reactions at module boundaries in the substrate networks, while simpler cofactors participate in widely generalized reactions. The highly tuned chemical structures of cofactors (sometimes exploiting distinctive properties of the elements of the periodic table) thereby act as 'keys' that incorporate classes of organic reactions within biochemistry.

Module boundaries provide the interfaces where change is concentrated, when we catalogue extant diversity of metabolic phenotypes. The same modules that organize the compositional diversity of metabolism are argued, with many explicit examples, to have governed long-term evolution. Early evolution of core metabolism, and especially of carbon-fixation, appears to have required very few innovations, and to have used few rules of composition of conserved modules, to produce adaptations to simple chemical or energetic differences of environment without diverse solutions and without historical contingency. We demonstrate these features of metabolism at each of several levels of hierarchy, beginning with the small-molecule metabolic substrate and network architecture, continuing with cofactors and key conserved reactions, and culminating in the aggregation of multiple diverse physical and biochemical processes in cells.

quarta-feira, dezembro 12, 2012

The frailty of adaptive hypotheses for the origins of organismal complexity

Michael Lynch *

Author Affiliations

Department of Biology, Indiana University, Bloomington, IN 47405

Abstract

The vast majority of biologists engaged in evolutionary studies interpret virtually every aspect of biodiversity in adaptive terms. This narrow view of evolution has become untenable in light of recent observations from genomic sequencing and population-genetic theory. Numerous aspects of genomic architecture, gene structure, and developmental pathways are difficult to explain without invoking the nonadaptive forces of genetic drift and mutation. In addition, emergent biological features such as complexity, modularity, and evolvability, all of which are current targets of considerable speculation, may be nothing more than indirect by-products of processes operating at lower levels of organization. These issues are examined in the context of the view that the origins of many aspects of biological diversity, from gene-structural embellishments to novelties at the phenotypic level, have roots in nonadaptive processes, with the population-genetic environment imposing strong directionality on the paths that are open to evolutionary exploitation.

Although biologists have always been concerned with complex phenotypes, the matter has recently become the subject of heightened speculation, as a broad array of academics, from nearly every branch of science other than evolutionary biology itself, claim to be in possession of novel insights into the evolution of complexity. The claims are often spectacular. For example, Kirschner and Gerhart (1) argue that evolutionary biology has been “woefully inadequate” with respect to understanding the origins of complexity and promise “an original solution to the long-standing puzzle of how small random genetic change can be converted into complex, useful innovations.” However, this book and many others like it (e.g., refs. 2–5) provide few references to work done by evolutionary biologists, making it difficult to understand the perceived areas of inadequacy, and many of the ideas promoted are known to be wrong, making it difficult to appreciate the novelty. Have evolutionary biologists developed a giant blind spot; are scientists from outside of the field reinventing a lot of bad wheels; or both?

Evolutionary biology is treated unlike any science by both academics and the general public. For the average person, evolution is equivalent to natural selection, and because the concept of selection is easy to grasp, a reasonable understanding of comparative biology is often taken to be a license for evolutionary speculation.It has long been known that natural selection is just one of several mechanisms of evolutionary change, but the myth that all of evolution can be explained by adaptation continues to be perpetuated by our continued homage to Darwin's treatise (6) in the popular literature. For example, Dawkins' (7–9) agenda to spread the word on the awesome power of natural selection has been quite successful, but it has come at the expense of reference to any other mechanisms, a view that is in some ways profoundly misleading. There is, of course, a substantial difference between the popular literature and the knowledge base that has grown from a century of evolutionary research, but this distinction is often missed by nonevolutionary biologists.

The goal here is to dispel a number of myths regarding the evolution of organismal complexity (Table 1). Given that life originated from inorganic matter, it is clear that there has been an increase in phenotypic complexity over the past 3.5 billion years, although long-term stasis has been the predominant pattern in most lineages. What is in question is whether natural selection is a necessary or sufficient force to explain the emergence of the genomic and cellular features central to the building of complex organisms.

terça-feira, dezembro 11, 2012

Michael Lynch:

…the uncritical acceptance of natural selection as an explanatory force for all aspects of biodiversity (without any direct evidence) is not much different than invoking an intelligent designer (without any direct evidence). True, we have actually seen natural selection in action in a number of well-documented cases of phenotypic evolution (Endler 1986; Kingsolver et al. 2001), but it is a leap to assume that selection accounts for all evolutionary change, particularly at the molecular and cellular levels.The blind worship of natural selection is not evolutionary biology. It is arguably not even science. Natural selection is just one of several evolutionary mechanisms, and the failure to realize this is probably the most significant impediment to a fruitful integration of evolutionary theory with molecular, cellular, and developmental biology.

There are limits on what selection can accomplish. We must remember that it merely acts as a sieve, preserving some variants and rejecting others; it does not create variation.If genetic change were random, what could ensure that enough favorable phenotypic variation had taken place for selection to have produced the exquisite adaptation and variety we see on the earth today?At various times, biologists thought that genetic change must be directed in some way to produce enough of the appropriate kinds of phenotypic variation. If selection were presented with a preselected subset of variants, that might greatly facilitate evolutionary change.Or if the organism generated just the right variants, selection might not be needed at all.Thus, the efficacy of selection would depend on the nature of phenotypic variation…Is genetic variation purely random, or is it in fact biased to facilitate evolutionary change?

Of the first of these approaches (e.g., Hoekstra and Coyne, 2007), I shall have nothing to say, as mechanistic developmental biology has shown that its fundamental concepts are largely irrelevant to the process by which the body plan is formed in ontogeny.In addition it gives rise to lethal errors in respect to evolutionary process. Neo-Darwinian evolution is uniformitarian in that it assumes that all process works the same way, so that evolution of enzymes or flower colors can be used as current proxies for study of evolution of the body plan. It erroneously assumes that change in protein coding sequence is the basic cause of change in developmental program; and it erroneously assumes that evolutionary change in body plan morphology occurs by a continuous process. All of these assumptions are basically counterfactual. This cannot be surprising, since the neo-Darwinian synthesis from which these ideas stem was a pre-molecular biology concoction focused on population genetics and adaptation natural history, neither of which have any direct mechanistic import for the genomic regulatory systems that drive embryonic development of the body plan.

…we know few of the principles that explain the ability of living things to innovate through a combination of natural selection and random genetic change. Random change by itself is not sufficient, because it does not necessarily bring forth beneficial phenotypes. For example, random change might not be suitable to improve most man-made, technological systems. Similarly, natural selection alone is not sufficient: As the geneticist Hugo de Vries already noted in 1905, ‘natural selection may explain the survival of the fittest, but it cannot explain the arrival of the fittest’. Any principle of innovation needs to explain how novel, beneficial phenotypes can originate. In other words, principles of innovation are principles of phenotypic variability.